Brash syndrome: Difference between revisions
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==Management== | ==Management== | ||
*Hyperkalemia treatment | |||
*Fluid resuscitation if hypovolemia | |||
==Disposition== | ==Disposition== | ||
Revision as of 18:00, 20 August 2019
Background
- Combination of following:
- Bradycardia
- Renal failure
- AV node blocker: beta-blocker, verapamil or diltiazem
- Shock
- Hyperkalemia
- Vicious cycle in setting of medications, hyperkalemia, renal failure
- Renal failure causes hyperkalemia and accumulation of AV node blockers, hyperkalemia synergizes with AV node blockers to cause bradycardia and hypoperfusion, hypoperfusion worsens renal failure [1]
Clinical Features
- Asymptomatic or symptomatic bradycardia
- Multisystem organ failure (shock, pulmonary edema, renal failure, shock liver)
- Altered mental status
Differential Diagnosis
- Differential bradycardia
- Differential renal failure
- pure hyperkalemia
- pure AV node blocker intoxication
Evaluation
- Brash syndrome patients can have mild hyperkalemia while pure hyperkalemia to cause bradycardia usually requires more dramatic elevation of potassium level
- ECG findings with bradycardia without other findings of hyperkalemia (QRS widening, peaked T waves) may favor BRASH
- pure AV blocker intoxication may or may not have hyperkalemia, need in BRASH. BRASH syndrome patients typically adherent to medications, not usually large ingestion
Management
- Hyperkalemia treatment
- Fluid resuscitation if hypovolemia
Disposition
See Also
External Links
References
- ↑ Hegazi MO, et al. Junctional bradycardia with verapamil in renal failure--care required even with mild hyperkalemia. J Clin PHarm Ther. 2012;37(6):726-8.
